Abstract
It has been postulated that the presence of parasites causing high extrinsic mortality may trigger an inducible acceleration of the host aging. We tested this hypothesis using isogenic populations of Caenorhabditis elegans nematodes and different Escherichia coli strains. When exposed to pathogenic bacteria, nematodes showed up to fourfold higher mortality rates, reproduced earlier, produced more H2O2, and accumulated more autofluorescence, than when exposed to an innocuous strain. We also observed that mortality increased at a slower rate in old animals, a phenomenon known as mortality deceleration. Mortality deceleration started earlier in populations dying faster, likely as a consequence of lifelong heterogeneity between individual tendencies to die. Taken together, our results strongly suggest that the high extrinsic mortality imposed by the pathogens results in the modulation of nematodes’ life-history traits, including aging and reproduction. This could be an adaptive response aiming at the maximization of Darwinian fitness.
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Acknowledgments
We thank Dennis Harris and Florence Cordier for reading the manuscript and helpful comments, Gregory Paul for expertise in statistics, Lydia Robert for expertise in mathematics, Jonathan Ewbank and members of his lab for technical assistance, and Ariel Lindner for expertise in fluorescence microscopy. This study was supported by ANR-06-BLAN-0406-01 to I. M., Nestle fellowship to M.L., and Servier Institute of Research fellowship to X.M.
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Table S1
Used oligonucleotides and plasmids. Oligonucleotides uvrA1 and uvrA2 were used to amplify by PCR a fragment from pKD13 that was used to replace the uvrA gene on the chromosome as described in (Datsenko and Wanner 2000), leading to strains IAI1 ΔuvrA::KanR and OP50 ΔuvrA::KanR.
Oligonucleotides lacZ1 and lacZ2 were used to amplify by PCR a fragment from pZA32 that was used to insert the yellow fluorescent protein gene under the control of the PLlacO promoter (Elowitz et al. 2002; Lutz and Bujard 1997) within the lac-operon on the chromosome as described in (Datsenko and Wanner 2000), leading to strain OP50 ΔlacZ::YFP-CmR. The insertion using oligonucleotides lacZ1 and lacZ2 also results in a LacI- phenotype (Lamerichs et al. 1989; Miller 1984; Miller and Schmeissner 1979), and therefore constant de-repression of the PLlacO promoter (Elowitz et al. 2002). (DOC 42 KB)
Fig. S1
Survival curves of C. elegans fed on different E. coli strains. †-symbol following the strain name indicates that UV-killed bacterial food was used throughout the life of the nematode. (EPS 410 KB)
Fig. S2
C. elegans mortality curves for all experimental conditions. Error bars represent 95% confidence intervals based on binomial distribution estimates; the errors are larger at the very beginning and end of every experiment due to the smaller number of events. A †-symbol following the strain name indicates that UV-killed bacterial food was used throughout the life of the nematode. (EPS 2024 KB)
Fig. S3
Correlation of fluorescent signal with the colony-forming unit (CFU) counts in intestinal content per nematode. The fluorescent signal reflects quite accurately the amount of living bacteria (R2=0.78, p<10−8). Photographs of nematodes fed on fluorescent OP50 were taken with a fluorescence microscope. Subsequently nematodes were crushed and intestinal content plated for quantification of living bacteria, i.e., CFUs. (EPS 503 KB)
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Baeriswyl, S., Diard, M., Mosser, T. et al. Modulation of aging profiles in isogenic populations of Caenorhabditis elegans by bacteria causing different extrinsic mortality rates. Biogerontology 11, 53–65 (2010). https://doi.org/10.1007/s10522-009-9228-0
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DOI: https://doi.org/10.1007/s10522-009-9228-0